Anesthesiology
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Technology for cardiac output (CO) and blood volume measurements has been developed based on blood dilution with a small bolus of physiologic body temperature saline, which, after transcardiopulmonary mixing, is detected with ultrasound sensors attached to an extracorporeal arteriovenous loop using existing central venous and peripheral arterial catheters. This study aims to compare the precision and agreement of this technology to measure cardiac output with a reference method, a perivascular flow probe placed around the aorta, in young children. The null hypothesis is that the methods are equivalent in precision, and there is no bias in the cardiac output measurements. ⋯ The technology to measure cardiac output with ultrasound detection of blood dilution after a bolus injection of saline yields comparable precision as cardiac output measurements by a periaortic flow probe. The difference in accuracy in the measured cardiac output between the methods can be explained by the coronary blood flow, which is excluded in the cardiac output measurements by the periaortic flow probe.
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This study hypothesized that, in experimental mild acute respiratory distress syndrome, lung damage caused by high tidal volume (VT) could be attenuated if VT increased slowly enough to progressively reduce mechanical heterogeneity and to allow the epithelial and endothelial cells, as well as the extracellular matrix of the lung to adapt. For this purpose, different strategies of approaching maximal VT were tested. ⋯ In experimental mild acute respiratory distress syndrome, lung damage in the shorter adaptation time group compared with the no adaptation time group was attenuated in a time-dependent fashion by preemptive adaptation of the alveolar epithelial cells and extracellular matrix. Extending the adaptation period increased cumulative power and did not prevent lung damage, because it may have exposed animals to injurious strain earlier and for a longer time, thereby negating any adaptive benefit.
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An airway manager's primary objective is to provide a path to oxygenation. This can be achieved by means of a facemask, a supraglottic airway, or a tracheal tube. If one method fails, an alternative approach may avert hypoxia. ⋯ Differentiation between failed laryngoscopy and failed intubation is important because the solutions differ. Failed facemask ventilation may be easily managed with an supraglottic airway or alternatively tracheal intubation. When alveolar ventilation cannot be achieved by facemask, supraglottic airway, or tracheal intubation, every anesthesiologist should be prepared to perform an emergency surgical airway to avert disaster.
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Chronic use of μ-opioid receptor agonists paradoxically causes both hyperalgesia and the loss of analgesic efficacy. Opioid treatment increases presynaptic N-methyl-D-aspartate receptor activity to potentiate nociceptive input to spinal dorsal horn neurons. However, the mechanism responsible for this opioid-induced activation of presynaptic N-methyl-D-aspartate receptors remains unclear. α2δ-1, formerly known as a calcium channel subunit, interacts with N-methyl-D-aspartate receptors and is primarily expressed at presynaptic terminals. This study tested the hypothesis that α2δ-1-bound N-methyl-D-aspartate receptors contribute to presynaptic N-methyl-D-aspartate receptor hyperactivity associated with opioid-induced hyperalgesia and analgesic tolerance. ⋯ α2δ-1-Bound N-methyl-D-aspartate receptors contribute to opioid-induced hyperalgesia and tolerance by augmenting presynaptic N-methyl-D-aspartate receptor expression and activity at the spinal cord level.